Increased urinary polyamine excretion after starting a very low calorie diet.

Urinary polyamine excretion has been suggested to reflect hypermetabolism or catabolism in different illnesses. In the present study, the excretion of urinary polyamines was examined in 12 obese subjects (3 men, 9 women aged 32-55 y, body mass index 33.3-64.

Differential effects of sepsis and trauma on urinary excretion of polyamines.

Urinary excretion of polyamines increases in patients with trauma and infection. To separate the effect of infection from the general metabolic response to sepsis, we studied 7 patients with sepsis and 13 patients with multiple trauma in the intensive-care unit. Urinary excretion of total and free polyamines, putrescine, spermidine, spermine, and their metabolites N1-acetylspermidine (N1-AcSPD) and N8-acetylspermidine (N8-AcSPD), and energy and nitrogen balance were measured.

Elevated seizure threshold and impaired spatial learning in transgenic mice with putrescine overproduction in the brain.

We have studied the role of putrescine by using transgenic mouse lines overexpressing the human ornithine decarboxylase gene in most of their tissues. The aberrant expression of the transgene is most strikingly manifested in the brain, leading to an increase of up to 20-fold in putrescine content. We report that the transgenic mice with grossly elevated putrescine in all brain regions analysed (cortex, striatum, hippocampus and cerebellum) showed a significantly elevated seizure threshold to chemical and electrical stimuli, and impaired performance in spatial learning and memory tests.

Transgenic mice over-producing putrescine in their tissues do not convert the diamine into higher polyamines.

We recently described a transgenic mouse line over-expressing the human ornithine decarboxylase gene virtually in all tissues. Despite strikingly elevated tissue putrescine concentrations, no or minimal changes were found in the levels of the higher polyamines spermidine and spermine. We have now extended these studies by further increasing tissue putrescine with the aid of 5-fluoromethylornithine, a specific inhibitor of ornithine transaminase and hence the catabolism of L-ornithine.

Methionine toxicity in the rat in relation to hepatic accumulation of S-adenosylmethionine: prevention by dietary stimulation of the hepatic transsulfuration pathway.

Rats were fed toxic levels of methionine with or without simultaneous dietary supplements of glycine and serine. Feed intake, growth rate, and metabolite concentrations in intestine, plasma, liver, skeletal muscle, and kidneys were monitored. Both toxic amounts of methionine and supplemental glycine and serine affected the tissue distribution of several amino acids resulting in similar, opposite, and diet-specific effects on the parameters studied.